Table of Contents  
REVIEW ARTICLE
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 55-59

Anti-thrombotic Regime for Percutaneous Intervention in Peripheral Arterial Disease: A Need of the Hour


1 Department of Pharmacology, M.S. Ramaiah Medical College, Bengaluru, Karnataka, India
2 Department of Vascular Surgery, M.S. Ramaiah Medical College, Bengaluru, Karnataka, India

Date of Web Publication31-Jul-2015

Correspondence Address:
Dr. Pallavi Kawatra
Department of Pharmacology, M.S. Ramaiah Medical College, Bengaluru, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-0820.161942

Rights and Permissions
  Abstract 

Peripheral arterial disease, a significant contributor to morbidity and mortality, is an imperative marker of a coexisting subclinical coronary artery disease. Since most of the patients become symptomatic at a later stage, a surgical approach becomes inevitable in these patients. With the introduction of percutaneous transluminal angioplasty, it has been possible to preclude numerous amputations. However, this procedure comes with the drawback of restenosis on the long term. In order to overcome this problem, a plethora of inconsistent regimes, pertaining to anti-thrombotics are being prescribed. In the face of the current scenario, to overcome the preordained outcome of restenosis, this systematic review highlights the problem of restenosis experienced in daily practice. It also discusses some commonly used anti-thrombotics and their success in various clinical trials suggesting the absolute need of a protocol for prescribing these drugs before and after angioplasty.

Keywords: Anti-thrombotics, percutaneous transluminal angioplasty, peripheral arterial disease, restenosis Anti-thrombotics, percutaneous transluminal angioplasty, peripheral arterial disease, restenosis


How to cite this article:
Kawatra P, Desai SC, Aiyappa C. Anti-thrombotic Regime for Percutaneous Intervention in Peripheral Arterial Disease: A Need of the Hour. Indian J Vasc Endovasc Surg 2015;2:55-9

How to cite this URL:
Kawatra P, Desai SC, Aiyappa C. Anti-thrombotic Regime for Percutaneous Intervention in Peripheral Arterial Disease: A Need of the Hour. Indian J Vasc Endovasc Surg [serial online] 2015 [cited 2021 May 7];2:55-9. Available from: https://www.indjvascsurg.org/text.asp?2015/2/2/55/161942


  Introduction Top


Peripheral arterial disease (PAD) can be described as a condition which comprises of the occlusion of peripheral arteries of the extremities and excludes the thoracic and intracranial vessels. It effects about 12% of the population in the United States. [1] Numerable factors such as atherosclerosis, instigated by the altered lifestyles, and various risk factors such as smoking, diabetes mellitus, hypertension result in narrowing of the arteries over a period of time. [2] Patients with PAD have approximately the same risk of death from cardiovascular diseases, as do patients with the history of coronary or cerebral vascular disease, the risk being particularly high in patients of large vessel disease. [3] Therefore, it may be considered as a surrogate marker of subclinical coronary artery diseases (CAD). PAD encompasses a broad spectrum of symptoms with which an individual may present, most frequently being intermittent claudication. [4] It is an ailment which effects the quality of life and interferes with the daily activities.

Options of both medical and surgical modalities are available in order to treat this condition. Drugs like statins, antiplatelet such as aspirin and clopidogrel, cilostazol are invariably given to these patients, [5] even though the prescription pattern may vary among physicians and surgeon. [6] With the introduction of promising surgical interventions, it has now been possible to forestall a number of amputations. Percutaneous transluminal angioplasty (PTA) has proven to be a useful modality in revascularization of iliac, femoropopliteal and below the knee arteries. Nevertheless, restenosis remains a limitation of this procedure which the surgeons stumble upon during a long term follow-up. This re-occlusion may be encountered as early as on the table while doing the procedure. According to a previous study significantly increased levels of thrombin-anti-thrombin III complexes, prothrombin fragments, and D-dimers are found even 1 h after PTA. [7] This systematic review has been formulated after an extensive search on PubMed and Google Scholar using keywords like anti-thrombotics and PTA in order to outline some commonly used anti-thrombotics by vascular surgeons. Unlike in cardiology, where a lot of trials have been conducted, there is not enough data to determine a protocol regarding the use of antiplatelet prior and after angioplasty for PADs.


  Role of Angioplasty in Peripheral Arterial Disease Top


Revascularization can be obtained by two types of procedures: Endovascular or surgery. Endovascular surgery includes angioplasty, stenting, and atherectomy. [8] PTA, is a technique whereby a catheter is inserted into the artery at the site of occlusion and the balloon is inflated in order to reinstate the patency of the vessel. Charles Theodore Dotter, also known as the father of intervention, revolutionized the treatment of peripheral atherosclerotic lesions with the introduction of the PTA in 1964. His first patient, Laura Shaw, was initially advised an amputation by her treating surgeon. However, when approached to Dotter, he considered the stenosis in the superficial femoral artery as a perfect model to test his catheter and eventually succeeded in making her walk on her feet. [9] Individuals with debilitating condition, unable to perform daily activities or suffering from critical limb ischemia are potential candidates for revascularization procedures. Peripheral percutaneous intervention is less invasive than open surgical bypass yet restore vessel patency, unlike pharmacotherapy. [10] It is suggested to be one of the primary options for treatment of infrainguinal arterial occlusive disease. [11] Though the success of this procedure may be subjected to various factors, a success rate of 90-95% has been attained so far for stenotic lesions and a slightly lower rate of 80-90% for complete occlusions. [12] It has been found to improve the 3 years overall survival rate up to 92.3% in one of the studies performed on 385 patients by Morris-Stiff et al. [13] However, re-occlusion is the main drawback encountered in the clinical practice since PTA induces a prothrombotic condition. The use of nitinol stents have been found to be superior to the conventional balloon angioplasty with better patency rates over a period of 12 months. [14],[15] Therefore, an appropriate regime of antiplatelet before and after the procedure becomes the need of the hour.


  Pathology of Restenosis Top


Restenosis is the recurrence of stenosis associated with the threshold for restenosis being >50%. It may be acute due to the formation of a blood clot or it may occur chronically over a period of time. This is essentially due to vascular injury occurring following the disruption of the atheromatous plaque during the procedure of angioplasty. The expansile force on the non-distensible plaque, results in its fragmentation, which initiates platelet deposition through the processes of platelet adhesion and recruitment of circulating platelets to form an enlarging mural platelet thrombus. Thrombin produced by simultaneous activation of the coagulation cascade by sub endothelial connective tissue structures enhances platelet deposition and stabilizes the forming thrombus with enmeshing fibrin. [16]

A number of factors may contribute to the occurrence of this restenosis such as the coexisting comorbidities, location of plaque, length of the segment effected, the vessel diameter, and the degree of occlusion. The narrower vessels are known to be more prone to stenosis in the long term. Simultaneously, an altered permeability leads to a direct interaction between the various components of the blood with vessel wall. [17]

Endothelium normally functions as a barrier to the various cellular components of the blood and even function to secrete PGI2 in order to prevent the platelets from aggregating. The role of PGI2 analogues on restenosis has already been demonstrated in animal models. [18] Thus, a direct injury to the vessel wall induces a denudation of the endothelial lining. It results in the exposure of the sub endothelial collagen which stems the release of adenosine diphosphate (ADP) and 5 hydroxytryptamine from the platelets resulting in an increase of their adhesion and aggregation. There is also a concomitant activation of the cox enzyme which leads to the production of thromboxane A2 and can contribute to the thrombus formation. An essential component of restenosis is the occurrence of intimal hyperplasia which is attributed to the various cells such as macrophages, mitogens, and growth factors like platelet derived growth factor (PDGF), which subsequently results in the reduction of the vessel compliance. Smooth muscle cells (SMCs) undergo phenotypic changes which are responsible for their proliferation. [19] In the initial phase of stenting, formation of thrombin-anti-thrombin complexes occurs, which signifies the activation of the coagulation cascade. The consequence of this is an increase probability of the occurrence of an early occlusion within 4 weeks of the intervention.


  Incidence of Restenosis Top


In a study done in 2003, where stenting was done for peripheral arteries, the range of restenosis following 1-year varied from 32% to 35%. [20] Although stenting decreases the incidence by 10%, the chances of in stent restenosis still remains high. Prevention of restenosis in the coronary vasculature has been demonstrated with cilostazol, trapidil, probucol, tranilast, nitric oxide donors, and clopidogrel. Given the similarities in revascularization procedures and in the pathophysiology of restenosis, it is possible that these results may be extrapolated to the setting of restenosis in the peripheral vasculature, making trials with these agents imperative. [21]


  Present Treatment Top


Aspirin

Aspirin is one of the oldest antiplatelet drugs which is known to be relegate the cardiovascular complications in patients of PAD. [22] As per the previous studies, use of aspirin is associated with a lower incidence of re-occlusion following PTA. However, due to the absence of any protocol, the dose to be used has not been standardized. One of the studies, which followed up about 207 patients for a period of 24 months, suggests that there is no marked difference in the efficacy between low dose and high dose aspirin. [23] In a meta-analysis of 287 studies, which compared the use of antiplatelet therapy against control, and even compared the different antiplatelet regimes, it was concluded that aspirin in a dose of 75-100 mg daily is effective in preventing episodes of occlusive vascular events in high risk patients. [24]

Clopidogrel

The Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance trial, which involved 15,603 patients suggested that the use of dual antiplatelet nay not significantly reduce the primary endpoint of myocardial infarction (MI) but may be beneficial to patients with a history of MI or ischemic stroke. [25] In the RELOAD study (the Reload with Clopidogrel before Coronary Angioplasty in Subjects Treated Long Term with Dual Antiplatelet Therapy) a loading dose of clopidogrel in patients already previously on clopidogrel, prior to coronary angioplasty resulted in a significant inhibition of platelet aggregation. [26] In one of the studies, treatment alone with a loading dose of 600 mg of clopidogrel, 6-24 h before the procedure has been shown to improve the clinical outcome over a period of 1-month due to its benefits in decreasing platelet reactivity. [27] This can provide a basis of evaluating the effects of clopidogrel for prevention of on table restenosis Clopidogrel might represent a useful alternative in cases in which aspirin is not tolerated or as a combination therapy with aspirin, especially when increased risk factors for re-occlusion are detected, although specific data on this strategy are lacking. [28] Clopidogrel pretreatment significantly reduces the incidence of cardiovascular death or ischemic complications both before and after percutaneous coronary intervention and without a significant increase in major or minor bleeding. [29]


  Dual Antiplatelet Therapy Top


Many interventionists use a combination of aspirin and clopidogrel before and after PTA and stenting in peripheral arteries. It has already been established that the use of dual platelets, aspirin along with clopidogrel combination is superior in patients of CAD undergoing stenting. However, according to a study conducted by Cassar et al., the use of loading dose of a combination of aspirin and clopidogrel in patients prior to angioplasty has found to inhibit the platelet function. [30] Dual antiplatelets decrease the ADP-stimulated fibrinogen binding and plasma PDGF but it does not have considerable effect on SMC proliferative capacity as measured by ERK 1/2 levels (extracellular regulated kinase-step of the mitogen-activated protein kinase cascade). [31]


  Cilostazol Top


In spite of its antiplatelet activity being known for more than two decades, not many trials have evaluated the efficacy of this novel phosphodiesterase inhibitor for prevention of re-occlusion following angioplasty. It is known to prevent both primary and secondary platelet aggregation unlike aspirin, which is known to inhibit only collagen induced platelet aggregation. [32] It decreases the level of circulating pro coagulants, thereby enhancing its antiplatelet activity. [33] Its role in prevention of restenosis can be attributed to the fact that it improves the endothelial function and therefore indirectly contributes to decreasing the activation of platelets in the circulation. [34] Tsuchikane et al. conducted a trial which emphasized on the role of this drug in preventing restenosis following percutaneous transluminal coronary angioplasty when compared with aspirin. [35] Its main role is due to inhibition of intimal hyperplasia, which is one of the foremost causes of restenosis. [36] Further, the up regulation of the hepatocyte growth factor as demonstrated in the Cilostazol for RESTenosis trial concluded its inevitable role in inhibition of abnormal proliferation of vascular smooth muscles. [37]


  Low Molecular Weight Heparin Top


Heparin is known to inhibit the intimal hyperplasia which is the major contributing factor to restenosis following angioplasty. However, in spite of its marked efficacy in animal models, its effect in clinical practice has been inconsistent. However, this incongruity in results has been ascribed to the difference in the dose and duration of treatment when compared with in vivo models. [38] The ERA study gaged the anti-proliferative effect of enoxaparin (a low molecular weight heparin) administered once daily for a period of 1-month following angioplasty. Despite the treatment being well-tolerated, it did not show any significant reduction in restenosis and did not alter the course of the clinical outcome. [39] Another alternative compound, dalteparin, prove to be unsuccessful in averting the complication of restenosis when evaluated in patients undergoing femoropopliteal PTA. [40]


  Present Guidelines Top


The RENDOVASC study highlighted the arbitrariness in the antiplatelet regime used in 1,557 patients following endovascular procedures in Spain. [41] A survey conducted at a national vascular meeting which included 51 respondents highlighted that majority of the surgeons prefer 81 mg of aspirin, though the duration of treatment was highly subjected to variation. [42] According to the 2014, European Society of Cardiology and the European Association for Cardio-thoracic Surgery guidelines on myocardial revascularization, a dual antiplatelet therapy is advised in patients of Acute Coronary Syndrome for a period of 1-year irrespective of the revascularization procedure. [43] However, due to a scarcity of sufficient data, such a protocol is lacking for patients of peripheral vascular disease undergoing PTA. As per the American College of Chest Physician guidelines, a single antiplatelet therapy is preferred for patients undergoing angioplasty whereas in patients with critical limb ischemia and rest pain, the use of prostanoids is recommended. [44] In recent article by Elias, it was henceforth put forward that though a dual antiplatelet may not be of any added benefit to patients of PAD undergoing revascularization, but it may be useful in patients of superficial femoral artery stenting. [45]


  Conclusion Top


At present, despite the lack of proper guidelines, antithrombotic treatments are being prescribed to patients of PAD undergoing PTA, on the basis of assessment of individual risk factors, the choice of stent and the profound clinical experience of various vascular surgeons. However, due to paucity of a universal protocol, there is inconsistency in the choice, dose as well as the duration of treatment. Thus, there lies an inevitable need to establish a consensus regarding the adequate regime for such patients in order to yield paramount results without any additional adverse effects.

 
  References Top

1.
Regensteiner JG, Hiatt WR. Treatment of peripheral arterial disease. Clin Cornerstone 2002;4:26-40.  Back to cited text no. 1
    
2.
Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FG, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007;45 Suppl S: S5-67.  Back to cited text no. 2
    
3.
Criqui MH, Langer RD, Fronek A, Feigelson HS, Klauber MR, McCann TJ, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992;326:381-6.  Back to cited text no. 3
    
4.
Ouriel K. Peripheral arterial disease. Lancet 2001;358:1257-64.  Back to cited text no. 4
    
5.
Aronow WS. Peripheral arterial disease of the lower extremities. Arch Med Sci 2012;8:375-88.  Back to cited text no. 5
    
6.
Klein-Weigel PF, Gutsche-Petrak B, Wolbergs S, Köning C, Flessenkamper I. Secondary medical prevention in patients with peripheral arterial disease-Prescriptions of vascular surgeons and medical doctors (angiologists) in a multidisciplinary vascular centre. Vasa 2010;39:145-52.  Back to cited text no. 6
    
7.
Tschopl M, Tsakiris DA, Marbet GA, Labs KH, Jäger K. Role of hemostatic risk factors for restenosis in peripheral arterial occlusive disease after transluminal angioplasty. Arterioscler Thromb Vasc Biol 1997;17:3208-14.  Back to cited text no. 7
    
8.
Jones WS, Schmit KM, Vemulapalli S, Subherwal S, Patel MR, Hasselblad V, et al. Treatment Strategies for Patients With Peripheral Artery Disease [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2013 May. Available from http://www.ncbi.nlm.nih.gov/books/NBK148574/ PubMed PMID: 23844447.  Back to cited text no. 8
    
9.
Payne MM. Charles Theodore Dotter. The father of intervention. Tex Heart Inst J 2001;28:28-38.  Back to cited text no. 9
    
10.
Nguyen LL. Percutaneous treatment of peripheral vascular disease: The role of diabetes and inflammation. J Vasc Surg 2007;45 Suppl A: A149-57.  Back to cited text no. 10
    
11.
Kudo T, Chandra FA, Ahn SS. The effectiveness of percutaneous transluminal angioplasty for the treatment of critical limb ischemia: A 10-year experience. J Vasc Surg 2005;41:423-35.  Back to cited text no. 11
    
12.
Davies MG, Waldman DL, Pearson TA. Comprehensive endovascular therapy for femoropopliteal arterial atherosclerotic occlusive disease. J Am Coll Surg 2005; 201:275-96.  Back to cited text no. 12
    
13.
Morris-Stiff G, Moawad M, Appleton N, Davies G, Hicks E, Davies C, et al. Long-term clinical outcome following lower limb arterial angioplasty. Ann R Coll Surg Engl 2011;93:250-4.  Back to cited text no. 13
    
14.
Laird JR, Katzen BT, Scheinert D, Lammer J, Carpenter J, Buchbinder M, et al. Nitinol stent implantation versus balloon angioplasty for lesions in the superficial femoral artery and proximal popliteal artery: Twelve-month results from the RESILIENT randomized trial. Circ Cardiovasc Interv 2010;3:267-76.  Back to cited text no. 14
[PUBMED]    
15.
Schillinger M, Sabeti S, Loewe C, Dick P, Amighi J, Mlekusch W, et al. Balloon angioplasty versus implantation of nitinol stents in the superficial femoral artery. N Engl J Med 2006;354:1879-88.  Back to cited text no. 15
    
16.
Harker LA. Role of platelets and thrombosis in mechanisms of acute occlusion and restenosis after angioplasty. Am J Cardiol 1987;60:20B-8.  Back to cited text no. 16
[PUBMED]    
17.
Cox JL, Gotlieb AI. Restenosis following percutaneous transluminal angioplasty: Clinical, physiologic and pathological features. CMAJ 1986;134:1129-32.  Back to cited text no. 17
[PUBMED]    
18.
Isogaya M, Yamada N, Koike H, Ueno Y, Kumagai H, Ochi Y, et al. Inhibition of restenosis by beraprost sodium (a prostaglandin I2 analogue) in the atherosclerotic rabbit artery after angioplasty. J Cardiovasc Pharmacol 1995;25:947-52.  Back to cited text no. 18
    
19.
Von Eckardstein A, editor. Atherosclerosis: Diet and Drugs. Berlin, Heidelberg: Springer Berlin Heidelberg; 2005. [Last cited on 2014 Nov 24]. Available from: http://link.springer.com/book/10.1007%2F3-540-27661-0   Back to cited text no. 19
    
20.
Becquemin JP, Favre JP, Marzelle J, Nemoz C, Corsin C, Leizorovicz A. Systematic versus selective stent placement after superficial femoral artery balloon angioplasty: A multicenter prospective randomized study. J Vasc Surg 2003;37:487-94.  Back to cited text no. 20
    
21.
Schainfeld RM. Potential emerging therapeutic strategies to prevent restenosis in the peripheral vasculature. Catheter Cardiovasc Interv 2002;56:421-31.  Back to cited text no. 21
    
22.
Poredos P, Jezovnik MK. Is aspirin still the drug of choice for management of patients with peripheral arterial disease? Vasa 2013;42:88-95.  Back to cited text no. 22
    
23.
Minar E, Ahmadi A, Koppensteiner R, Maca T, Stümpflen A, Ugurluoglu A, et al. Comparison of effects of high-dose and low-dose aspirin on restenosis after femoropopliteal percutaneous transluminal angioplasty. Circulation 1995;91:2167-73.  Back to cited text no. 23
    
24.
Antithrombotic Trialists′ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86.  Back to cited text no. 24
[PUBMED]    
25.
Bhatt DL, Topol EJ, Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance Executive Committee. Clopidogrel added to aspirin versus aspirin alone in secondary prevention and high-risk primary prevention: Rationale and design of the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA) trial. Am Heart J 2004;148:263-8.  Back to cited text no. 25
    
26.
Collet JP, Silvain J, Landivier A, Tanguy ML, Cayla G, Bellemain A, et al. Dose effect of clopidogrel reloading in patients already on 75-mg maintenance dose: The Reload with Clopidogrel Before Coronary Angioplasty in Subjects Treated Long Term with Dual Antiplatelet Therapy (RELOAD) study. Circulation 2008;118:1225-33.  Back to cited text no. 26
    
27.
Cuisset T, Frere C, Quilici J, Morange PE, Nait-Saidi L, Carvajal J, et al. Benefit of a 600-mg loading dose of clopidogrel on platelet reactivity and clinical outcomes in patients with non-ST-segment elevation acute coronary syndrome undergoing coronary stenting. J Am Coll Cardiol 2006;48:1339-45.  Back to cited text no. 27
    
28.
Visonà A, Tonello D, Zalunardo B, Irsara S, Liessi G, Marigo L, et al. Antithrombotic treatment before and after peripheral artery percutaneous angioplasty. Blood Transfus 2009;7:18-23.  Back to cited text no. 28
    
29.
Sabatine MS, Cannon CP, Gibson CM, López-Sendón JL, Montalescot G, Theroux P, et al. Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics: The PCI-CLARITY study. JAMA 2005;294:1224-32.  Back to cited text no. 29
    
30.
Cassar K, Ford I, Greaves M, Bachoo P, Brittenden J. Randomized clinical trial of the antiplatelet effects of aspirin-clopidogrel combination versus aspirin alone after lower limb angioplasty. Br J Surg 2005;92:159-65.  Back to cited text no. 30
    
31.
Wilson AM, Brittenden J, Bachoo P, Ford I, Nixon GF. Randomized controlled trial of aspirin and clopidogrel versus aspirin and placebo on markers of smooth muscle proliferation before and after peripheral angioplasty. J Vasc Surg 2009;50:861-9.  Back to cited text no. 31
    
32.
Kimura Y, Tani T, Kanbe T, Watanabe K. Effect of cilostazol on platelet aggregation and experimental thrombosis. Arzneimittelforschung 1985;35:1144-9.  Back to cited text no. 32
    
33.
Rao AK, Vaidyula VR, Bagga S, Jalagadugula G, Gaughan J, Wilhite DB, et al. Effect of antiplatelet agents clopidogrel, aspirin, and cilostazol on circulating tissue factor procoagulant activity in patients with peripheral arterial disease. Thromb Haemost 2006;96:738-43.  Back to cited text no. 33
    
34.
Goto S. Cilostazol: Potential mechanism of action for antithrombotic effects accompanied by a low rate of bleeding. Atheroscler Suppl 2005;6:3-11.  Back to cited text no. 34
    
35.
Tsuchikane E, Fukuhara A, Kobayashi T, Kirino M, Yamasaki K, Kobayashi T, et al. Impact of cilostazol on restenosis after percutaneous coronary balloon angioplasty. Circulation 1999;100:21-6.  Back to cited text no. 35
    
36.
Tsuchikane E, Katoh O, Sumitsuji S, Fukuhara A, Funamoto M, Otsuji S, et al. Impact of cilostazol on intimal proliferation after directional coronary atherectomy. Am Heart J 1998;135:495-502.  Back to cited text no. 36
    
37.
Morishita R. A scientific rationale for the CREST trial results: Evidence for the mechanism of action of cilostazol in restenosis. Atheroscler Suppl 2005;6:41-6.  Back to cited text no. 37
    
38.
Buchanan MR, Brister SJ. Inhibition of chronic vessel wall intimal hyperplasia following acute anticoagulant treatment: Relative effects of heparin and dermatan sulphate. Thromb Res 1998;91:157-67.  Back to cited text no. 38
    
39.
Faxon DP, Spiro TE, Minor S, Coté G, Douglas J, Gottlieb R, et al. Low molecular weight heparin in prevention of restenosis after angioplasty. Results of Enoxaparin Restenosis (ERA) Trial. Circulation 1994;90:908-14.  Back to cited text no. 39
    
40.
Koppensteiner R, Spring S, Amann-Vesti BR, Meier T, Pfammatter T, Rousson V, et al. Low-molecular-weight heparin for prevention of restenosis after femoropopliteal percutaneous transluminal angioplasty: A randomized controlled trial. J Vasc Surg 2006;44:1247-53.  Back to cited text no. 40
    
41.
Matas M, Domínguez González JM, Montull E. Antiplatelet therapy in endovascular surgery: The RENDOVASC study. Ann Vasc Surg 2013;27:168-77.  Back to cited text no. 41
    
42.
Allemang MT, Rajani RR, Nelson PR, Hingorani A, Kashyap VS. Prescribing patterns of antiplatelet agents are highly variable after lower extremity endovascular procedures. Ann Vasc Surg 2013;27:62-7.  Back to cited text no. 42
    
43.
Kolh P, Windecker S, Alfonso F, Collet JP, Cremer J, Falk V, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur J Cardiothorac Surg 2014;46:517-92.  Back to cited text no. 43
    
44.
Alonso-Coello P, Bellmunt S, McGorrian C, Anand SS, Guzman R, Criqui MH, et al. Antithrombotic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9 th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:e669S-90.  Back to cited text no. 44
    
45.
Hanna EB. Dual antiplatelet therapy in peripheral arterial disease and after peripheral percutaneous revascularization. J Invasive Cardiol 2012;24:679-84.  Back to cited text no. 45
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
   Abstract
  Introduction
   Role of Angiopla...
   Pathology of Res...
   Incidence of Res...
  Present Treatment
   Dual Antiplatele...
  Cilostazol
   Low Molecular We...
  Present Guidelines
  Conclusion
   References

 Article Access Statistics
    Viewed2605    
    Printed59    
    Emailed0    
    PDF Downloaded83    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]